Anticonvulsant,antiepileptogenic, and antiictogenic pharmacostrategies

Pharmacological concepts tailored to status epilepticus, to epileptogenesis following acquired brain insults, and to ictogenesis in established epilepsy vary considerably and should ideally be directed at those pathophysiological mechanisms that presumably underly these conditions. Currently known important molecular targets include voltage-gated sodium and calcium channels, the γ-aminobutyric acid (GABA) system and ionotropic glutamate receptors. Metabotropic glutamate receptors, potassium channels, and neurotransmitters such as acetylcholine, glycine, and monoamines are beyond the scope of this review. In status epilepticus, immediate failure of GABAergic inhibition occurs, and administration of benzodiazepines and barbiturates displays the pharmacostrategic mainstay. In epileptogenesis within limbic structures, the most important underlying pathophysiological mechanisms currently discussed are transient loss of inhibition and aberrant mossy fiber sprouting. Both processes may be facilitated by N-methy-d-aspartat (NMDA) receptor regulation. NMDA antagonists may exhibit antiepileptogenic properties in experimental animals, but reliable data in humans are lacking. In established epilepsy, voltage-gated ion channels and impairment of GABAergic functions contribute to mechanisms facilitating ictogenesis. Blockade of sodium and calcium channels and enhancement of GABAergic inhibition are currently the most important tools to prevent the occurrence of seizures. Received 16 January 2007; received after revision 7 March 2007; accepted 17 April 2007     

Rulkov神经元的的簇放电类型与分岔条件

讨论了Rulkov神经元产生锥形簇放电、方形簇放电及峰放电的非线性动力学特征,尤其是锥形簇放电的放电规律和动力学特征。指出产生锥形簇放电的关键在于鞍结点分岔和flip分岔,属于fold/flip型簇放电;而锥形簇放电的持续距离随着控制参数的增加而增大。首次给出了单个神经元产生各种簇放电的参数取值范围。     

硅表面改性及其生物学研究

为了增加海马神经元在以硅为基底的微电子器件表面的黏附和生长,采用化学方法对集成电路的衬底材料硅进行了表面改性,并对改性前后的硅表面进行了x射线光电子能谱分析、原子力显微镜形貌分析和接触角测定.用改良的考马斯亮蓝法对硅片和改性后的硅片进行了蛋白质吸附研究,并采用荧光显微镜观察了胎鼠海马神经细胞在改性前后硅表面的黏附行为.结果表明,改性后的硅表面接触角减小,粗糙度增加.蛋白质吸附结果表明硅的改性能减少蛋白质的吸附.海马神经细胞在改性硅前后表面的黏附行为研究表明,未改性的硅片上几乎不能黏附海马神经细胞,而改性后硅片上能显著增加海马神经细胞的黏附和生长,并能形成神经细胞网络.     

单神经元自适应PID控制器的研究

将二次型性能指标引入单神经元并利用自学习功能构成了自适应ＰＩＤ控制器;分析了神经元自适应控制系统的稳定性和学习算法的收敛性。仿真结果表明,这种控制方案具有良好的自适应性。     

Differential insult-dependent recruitment of the intrinsic mitochondrial pathway during neuronal programmed cell death

Programmed cell death contributes to neurological diseases and may involve mitochondrial dysfunction with redistribution of apoptogenic proteins. We examined neuronal death to elucidate whether the intrinsic mitochondrial pathway and the crosstalk between caspase-dependent/-independent injury was differentially recruited by stressors implicated in neurodegeneration. After exposure of cultured cerebellar granule cells to various insults, the progression of injury was correlated with mitochondrial involvement, including the redistribution of intermembrane space (IMS) proteins, and patterns of protease activation. Injury occurred across a continuum from Bax- and caspase-dependent (trophic- factor withdrawal) to Bax-independent, calpain-dependent (excitotoxicity) injury. Trophic-factor withdrawal produced classical recruitment of the intrinsic pathway with activation of caspase-3 and redistribution of cytochrome c, whereas excitotoxicity induced early redistribution of AIF and HtrA2/Omi, elevation of intracellular calcium and mitochondrial depolarization. Patterns of engagement of neuronal programmed cell death and the redistribution of mitochondrial IMS proteins were canonical, reflecting differential insult-dependencies. Received 14 August 2008; received after revision 02 October 2008; accepted 23 October 2008     

听中枢神经元频率选择性形成的机制:near-CF还是off-CF?

已知从外周到初级听皮层,神经元的频率选择性逐级提高,然而,有关该过程的神经机制长期以来一直处于争论之中．本文对这一核心问题进行了分析与探讨。     

腺苷诱导神经细胞Ca~(2+)响应的微孔板荧光检测

以钙离子荧光指示剂Fluo-3-AM作为神经细胞内Ca2+荧光探针,用微孔板荧光检测仪测量神经细胞内游离Ca2+与荧光探针Fluo-3-AM结合的荧光强度,并实时检测此荧光强度在细胞外加不同浓度腺苷诱导下的变化情况。实验发现,各种浓度的腺苷都能诱导神经细胞Ca2+浓度升高,且其影响程度随腺苷浓度的增大而增强。这一结果对探究腺苷通过作用神经系统起止痛作用的机理具有重要意义。     

三七总皂苷对新生大鼠海马神经干细胞活性影响及促分化作用

目的研究三七总皂苷对海马神经干细胞活性的影响和分化作用。方法体外培养海马神经干细胞,分别接种于96孔板和12孔板,96孔板细胞按三七总皂苷不同浓度梯度和同一浓度的不同时间点进行干预,应用MTT法检测海马神经干细胞的OD值,观察三七总皂苷对海马神经干细胞活性的影响;12细胞孔板分为对照组和给药组,应用免疫荧光染色方法检测神经元新生特异抗原（Tuj-1）和胶质细胞新生抗原（Vimentin）的表达,以观察三七总皂苷对海马神经干细胞分化的影响。结果（1）一定浓度范围内三七总皂苷能增强海马神经干细胞活性;（2）三七总皂苷能促进海马神经干细胞向神经元和胶质细胞方向分化。结论三七总皂苷能增强海马神经干细胞的活性并能促进海马神经干细胞分化。     

跨越连接多层神经网络的稳定性

研究了跨越连接多层神经网络的结构和稳定性。提出了有跨越连接的误差反向传播算法,通过仿真实验说明了跨越连接多层神经网络收敛性和稳定性优于传统网络。     

双斑蟋腹末神经节内DUM神经元的神经支配

应用活体染色法和氯化镍逆行染色法研究双斑蟋(Gryllus bi maculatus)(1773,DeGeer)腹末神经节内已确定的DUM神经元具体的神经支配,结果表明:DUM神经元的轴突主要经N3-3到达输卵管,经N5-3到达输卵管,经N7-1到达M4肌,M5肌,M6肌和M7肌.